NF-κB
When cells are exposed to damaging stimuli, the protein NF-κB is immediately activated and has been linked to a wide range of inflammatory illnesses. Inflammation and innate immunity are both affected by this protein complex, which controls DNA transcription. The NF-κB pathway is activated by TLRs, TNF receptors, and IL receptors recognizing different PAMPS and DAMPS (Okada & Suzuki, 2017). Because it regulates the development of a vasoconstrictor, NF-κB signaling and its downstream cytokine products are crucial to the pathophysiology of SAH. Using various drugs to inhibit NF-κB activity, several authors have observed improved neurological scores, decreased neuronal death, reduced BBB permeability, and lower inflammatory cytokines following SAH. (Chang, Wu, Lin, Hwang & Kwan, 2012; Liu, Yang, Pan, Liu & Ma, 2016; Zhang et al., 2015) , Future research on NF-κB is promising, and the usefulness of employing this molecule as a therapeutic target in the treatment of SAH in humans needs to be determined. In the study by Liu et al. (Liu et al., 2016) Matrine was found to reduce EBI in rats following subarachnoid hemorrhage by inhibiting NF-κB via PI3K/Akt and inducing HO-1 via Keap1/Nrf2.